Atria of the Heart

Most species of animals rely on a well-organized circulatory system to move blood and nutrients around the body. The heart is a critical component of the human (and other animals’) circulatory system. While each aspect of the heart plays an important role in the circulatory system, the atria are particularly important as they help to fill the ventricles prior to ventricular contraction.

As such, the goal of this article is to discuss the embryology, anatomy, and blood supply of the atria of the heart. Furthermore, the physiological function, as well as pathological conditions affecting the atria will also be addressed.

Basic Anatomy of the Heart

The heart is at the center of this system, as it pumps blood through vascular channels towards the target tissue. Recall that the heart is a roughly pyramidal organ made up of two muscular pumps that are connected in-series – namely, the left and rightheart. Each pump contains an upper chamber that functions as a receptacle for incoming blood, called the atrium, and a lower chamber that is responsible for pushing blood out of the heart called the ventricle. The heart is located in the mediastinum within a region known as the cardiac box; the boundaries of which include:

an imaginary line passing through the jugular notch superiorly,

a parallel line passing through the xiphoid process inferiorly,

bilaterally are two imaginary vertical lines, each passing through the respective left and right midclavicular lines (or nipple line in the non-pendulous breast).

Overview of the heart in situ - ventral view

Within this space, the heart is oriented obliquely, with the true cardiac apex pointing anteroinferiorly to the left. The surface that the heart rests on in vivo is not the true cardiac base, but rather it is the diaphragmaticsurface. The anatomical base points dorsally and slightly upwards to the right. The right atrium and ventricle make up most of the sternocostalsurface of the heart, while the diaphragmatic surface is made up by the right and left ventricles. The left atrium contributes to the anatomical base.

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Heart in situ seen from the anterior view.

The heart contains three main layers of tissue. The innermost layer is known as the endocardium and the outermost layer is the epicardium. Between those two layers is a thick layer of specialized (i.e. cardiomyocytes) known as the myocardium. The thickness of the myocardium varies between regions of the heart. In the absence of underlying pathology, the ventricles are always thicker than the atria. Furthermore, the left chambers are thicker than the right counterparts, owing to the fact that the former has to pump blood against greater resistance when compared to the lower pulmonary resistance that the right chambers have to overcome.

Although all blood – both nutrient-rich oxygenated and nutrient-poor deoxygenated – passes through the heart, the thickness of the heart walls reduces efficient transport of essential nutrients to the cardiac tissue. As a result, the heart has its own circulatory network known as the coronary arteries and veins. The coronary arteries are a paired set of vessels arising from the base of the ascending aorta. Each vessel arborizes to give numerous branches that supply all layers of the heart. There are several venous tributaries as well that eventually drain deoxygenated blood from the layers of the heart and return it mainly to the right atrium; however, some vessels have been shown to drain to the right ventricle, and less commonly to the left heart.

Embryology of the Atria

As early as the third week of gestation, the cardiovascular system begins to develop. The primordial heart begins to take shape halfway through weekthree of gestation. Note that this coincides with the fact that the developing embryo is becoming more complexed and as such, can no longer be adequately supplied by simple diffusion of nutrients. At this time the heart is a continuous tube with primitive connections.

At the midpoint of the fourth gestational week, internal differentiation begins to take place, resulting in the formation of primordial atria and ventricles. Entities such as bone morphogenetic proteins 2A and 4 (BMP-2A & BMP-4), transforming growth factor beta one and two (TGF- β1 & TGF- β2), and other inductive agents promote the differentiation of cardiacjelly (a specialized type of extracellular matrix) into the endocardialcushions. These cushions appear on the ventral and dorsal walls of the atrioventricular canal during the fifth gestational week. As the heart continues to develop, the endocardial cushions are populated by mesenchyme. Consequently, the opposing endocardial cushions begin to abut, and eventually fuse with each other. This leads to the formation of left and right atrioventricularcanals; with the endocardial cushions both acting as a valve (to limit regurgitant streams from the ventricles to the atria) and to separate the atria from the ventricles.

Concurrently, the primitive interatrial septa also begin to form during the 4th gestational week. Initially, a thin moon-shaped membranous structure begins to form from the roof of the primordial atria to the endocardial cushion. This early wall is known as the septumprimum (i.e. primary septum); it partially separates the atria into the left and right components. The free crescentic edge of the septum primum, along with the superior border of the endocardial cushion, provides superior and inferior (respectively) boundaries for the foramenprimum (i.e. the first foramen). It acts as a physiological shunt that allows oxygenated blood to pass into the left atrium. Over time, the septum primum continues to proliferate and fuse with the endocardial cushions, thus obliterating the foramen primum.

Embryonic atrial heart valves

During the time that the lower part of the septum primum begins to fuse, fenestrations begin to appear in the middle of the membrane. These fenestrations, which originated following several apoptotic signals to the septum primum, coalesce to form the foramensecundum (i.e. the second foramen). This opening maintains the physiological right to left shunt that was created with the foramen primum. Between the 5th and 6th gestational weeks, a thicker crescentic muscular membrane, known as the septumsecundum (i.e. the second septum) originates in the roof of the right atrium and grows caudally where it gradually covers the foramen secundum. Although the septum secundum completely covers the foramen secundum, the inferodorsal aspect of the membrane remains incomplete. The septal defect that remains is oval in shape and is therefore referred to as the foramenovale (i.e. the oval foramen). Simultaneously, the cranial part of the septum primum undergoes apoptotic degeneration, resulting in the obliteration of the foramen secundum. The foramen ovale now functions as the pathway for the physiological right to left shunt. The remaining caudal part of the septum primum acts as a valve to prevent premature reversal of the shunt; it is therefore referred to as the valve of the foramen ovale.

Valve of foramen ovale - lateral-left view

Prior to the development of the sinoatrialnode, the automaticity of the heart is regulated by the primordial atrial myocardium. During the 5th gestational week, the sinoatrial node begins to develop within the walls of the right sinus venosus. As the sinus venosus becomes incorporated into the wall of the right atrium, the sinoatrial node also migrates to its final location near the orifice of the superior vena cava.

Under normal circumstances, shortly after birth, the increase in systemic pressure relative to that of the pulmonary pressure results in an overall increase in the pressures in the left side of the heart. Since the left atrial pressure becomes greater than that in the right atrium, it forces the overlapping membranes together. By the third month of extrauterine life, the septum secundum and the valve of the foramen ovale would have fused, leaving only the fossa ovalis as a remnant.

Fossa ovalis of the heart - lateral-right view

Anatomy of the Atria

Much like the wide, open architectural atrium that functions as receiving sites for incoming guests, the cardiac atrium is a pair of chambers situated at the upper part of the heart that receives systemic and pulmonary blood. The rightatrium receives deoxygenated blood from the systemic circulation via the superior and inferior vena cava. On the other hand, oxygenated blood leaving the lungs is carried to the leftatrium via the pulmonary veins.

In the anatomical position, the left atrium is concealed behind the right atrium, as the latter contributes to most of the upper part of the sternocostal surface of the heart. The interatrialgroove (which is the surface marking for the atrial septum) serves as a landmark that separates the atria on the surface of the heart. It continues toward the posterior surface of the heart where it meets the atrioventricular and posterior interventricular grooves at the cardiac crux.

The left and right atria are separated by a fibromuscular wall known as the atrial (interatrial) septum, while the ventricles are separated by a similar structure, known as the ventricular (interventricular) septum. Additionally, each atrium is separated from the ventricle of the same side by the atrioventricularseptum. However, unlike the interventricular and interatrial septa, the atrioventricular septum are fitted with valves (i.e. left and right atrioventricular valves) that allow blood to move from the upper to the lower chambers. These valves also promote a unidirectional flow of blood through the heart, as under normal circumstances, they prevent reflux of blood during ventricular contraction.

The Left Atrium

The left atrium is positioned slightly above and behind the right atrium. Although it is smaller in terms of the amount of blood it can hold, the left atrium has a thicker myocardial wall when compared to the right atrium. This is a result of the fact that the left atrium is exposed to higher pressures – and therefore does more work – than the right atrium. Like the right atrium, the cuboidal left atrial wall is made up of venous entities (in addition to auricular and vestibular parts as well). In this case, the four ostia of the pulmonary veins enter the posterior aspect of the left atrium. The vessels pierce either side of the posterior wall (which also contributes to the majority of the anatomical base of the heart) in pairs.

Left atrial appendage - anterior view

Most of the anterior surface of the left atrium is concealed behind the roots of the emerging great vessels. Furthermore, part of the transverse pericardial sinus (the space between the superior vena cava [posteriorly] and the great trunks of the great arteries [anteriorly]) passes in front of the left atrium as well. The left atrium also has an auricularappendage; however, it is more slender than its right counterpart and is also curved distally as it partially overlaps the trunk of the pulmonary artery.

Structures Surrounding the Left Atrium

In the anatomical position, the left atrium is located between the 5th to 8th thoracic vertebrae if the individual is supine (lying flat) or the 6th to 9th vertebrae in someone who is standing erect. Also posteriorly related to the left atrium are the descending aorta, esophagus, and the previously described pulmonary veins.

Overview of the left atrium and ventricle

Internal Features of the Left Atrium

Like the right atrium, the venous aspect of the inner left atrium is smooth and boasts theostia of the four pulmonary veins in the cranial posterolateral aspect of the atrial wall. While four openings are usually seen in most cases, the left set of pulmonary veins may also emerge in a common conduit. The auricular surface is also highly trabeculated (as seen in the right atrium) as the left atrial auricle contains all the pectinate muscles found within the left atrium.

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Definition, function and anatomy of the left atrium.

The Right Atrium

The outer walls of the right atrium contribute to the convexity of the right pulmonary surface, the upper right part of the anatomical base, and the upper anterior surface of the heart. The dome of the atrium is pierced by the superior vena cava, while the posteroinferior part receives the inferior vena cava. A triangular, muscular sac known as the right auricle (right atrial appendage) extends anteriorly and to the left, partially covering the base of ascending aorta.

The basal surface of the right atrium also has a shallow depression known as the sulcus terminalis. It marks the point of fusion between the venous part of the right atrium (formed by the sulcus venosus) and the true right atrium. The sulcus terminalis also provides a surface marking for the crista terminalis (terminal crest), which serves as the origin for the pectinate muscles that extend perpendicularly.

Structures Surrounding the Right Atrium

The lateralside of the right atrium is adjacent to the mediastinal surface of the right lung. However, the hilum of the right lung is slightly posterior to this aspect of the right atrium. Intervening between the right lung and ipsilateral atrium are the pericardium, pericardiophrenic vessels, right phrenic nerve, and pleura. Posterolaterally to the right of the right atrium is the right pulmonary veins, while the associated interatrial groove is located posteriorly and to the left of the right atrium. The anterior mediastinal aspect of the right lung is anteriorly related to the right atrium. The structures separating the two are the pleura and pericardium.

Overview of the right atrium and ventricle

The sinoatrialnode, which is responsible for regulating the automaticity of the myocardium, is located in the posterior wall of the right atrium. More specifically, it is inferolateral to the opening of the superior vena cava, along the superior part of the crista terminalis. The secondary cardiac pacemaker – the atrioventricularnode – is situated in the inferior aspect of the right atrium, within the triangle of Koch. Of note, the triangle of Koch is limited by the coronary sinus, the septal cusp of the tricuspid valve, and the tendon of Todaro.

Internal Features of the Right Atrium

Based on the embryological origins of the right atrium, the internal surface can be subdivided into the venous, vestibular, and auricularsurfaces. They can be macroscopically distinguished from each other based on the fact that the auricular part has a trabeculated appearance (due to the overlapping pectinate muscles), the venous part is smooth, and the vestibular part is rigid. While the vestibular and auricular surfaces are derivatives of the primordial atrium proper, the venous compartment is the remnant of the sinus venosus. The latter fuses with the right atrium, thus merging the vena caval ostia with the posterior wall of the right atrium.

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Definition, function and anatomy of the right atrium.

While numerous minor venous tributaries drain directly into the right atrium, the principal afferents to the right atrium are the venae cavae and the coronary sinus. On occasion, the right marginal and anterior cardiac veins may open directly into the right atrium as well. The inferior vena cava and coronary sinus are the only two vessels draining into the right atrium that have valvular mechanisms to prevent venous reflux.

The Eustachian valve is the valve of the inferior vena cava, while the Thebesianvalve is the valve of the coronary sinus. The valve of the inferior vena cava is anteriorly related to the opening of the vein. It travels along the right border of the vessel and traverses the sinus septum (partition between the oval fossa [fossa ovale] and the coronary sinus) inferiorly; after which it merges with the valve of the coronary sinus. The thin, semi-circular Thebesian valve continues from its attachment with the Eustachian valve, toward the round tendon of Todaro. Of note, the tendon of Todaro is attached proximally at the sinus septum and inserts into the central fibrous body (strongest part of the cardiac skeleton).

Functions of the Atria

Both atria carry out three distinct functions in an ordered sequence. While the ventricles are contracting and the atrioventricular valves are closed, blood still continuously flows from the venae cavae on the right, and the pulmonary veins on the left, to fill the atria. During this phase, the atria act as reservoirs that store blood temporarily.

Once ventricular contraction stops and the pressure within the atria overcomes the pressure within the ventricles, the atrioventricular valves open and the blood passes into the ventricles. This passivephase of ventricular filling accounts for roughly 80% of the ventricular volume at the beginning of systole. Keep in mind also, that while the atrioventricular valves are open, blood is still draining into the atria from their respective veins.

Once the heart has recovered from the electrical refractory period (i.e. repolarization is complete), the sinoatrial node initiates the action potential required to generate atrial contraction. Both atria contract simultaneously and the remaining 20% of the ventricular volume is activelypumped into the ventricles.

Disorders of the Atria

While the atria are important for temporarily storing blood and priming the heart, the majority of the work done by the heart is carried out by the ventricles. Therefore, most cases of atrial dysfunction may go relatively unnoticed until the individual attempts strenuousactivities. Nevertheless, there are quite a few disorders that affect the atria; however, most of them are secondary to valvular or ventricular dysfunction.

The major congenital problems associated with the atria are septaldefects. Other congenital problems include abnormalelectricalcircuits in the atria that can result in supraventriculartachycardia. The acquired disorders include atrialarrhythmias, which may be the consequence of atrial dilatation and enlargement.

Atrial Septal Defects

Atrial septal defects refer to abnormal communications between the upper cardiac chambers. Recall that during intrauterine life, a physiological shunt exists where oxygenated blood (from the mother) enters the right atrium and passes via the foramen ovale (or foramen primum and foramen secundum prior to the 8th gestational week) to the left atrium in order to be passed to the left ventricle and distributed throughout the foetal circulation. Under normal circumstances, these communications will close off within three months of extrauterine life. If there is an atrial septal defect, then initially blood will flow from the left atrium to the right. This typically isn’t associated with significant morbidity as the mixed blood is destined for the lungs, where it will be adequately oxygenated. Unfortunately, over time, the right atrium will be exposed to relatively higher pressures and its myocardium will hypertrophy. If the right atrial pressure exceeds the left atrial pressure, the shunt will be reversed (right to left). Consequently, blood with lower oxygen saturation will be pumped into the systemic circulation and the individual is likely to experience symptoms of hypoxemia.

The genetic basis of atrial septal defects is well documented. Syndromic abnormalities such as DiGeorge (microdeletion of 22q11.2), Down (trisomy 21), and Ellis-van Creveld (mutation of 4p16 that is also known as chondroectodermal dysplasia) syndromes have all been associated with atrial septal defects. While they are commonly diagnosed in childhood, it is not uncommon to see adults also presenting with atrial septal defects. They are the most common types of congenital cardiac anomalies, alongside the valvulopathies. Six out of ten patients who present with an atrial septal defect are females. The most common type of atrial septal defects is the patent ostium secundum, followed by patent foramen ovale. Other atrial septal defects include persistent ostium primum on the background of an endocardial cushion defect, sinus venosus, and common atrium.

The pathogenesis can be narrowed down to one of the following problems:

Abnormal absorption of the septum primum where the incorrect part or too much of the septum was reabsorbed can give rise to a patent foramen ovale. An abnormally large foramen ovale can also persist due to the fact that it will not be adequately occluded by the remaining septum primum .

Failure of the septum secundum to form adequately and occlude the ostium secundum may result in the defect persisting into extrauterine life.

If the endocardial cushions fail to fuse, then the ostium primum will remain patent since the septum primum has nothing to merge with. This is the most likely cause of endocardial cushion defects with ostium primum .

Sinoatrial Node Disorders

The autonomic nervous system works in tandem to regulate the activities of the sinoatrialnode. The heart is said to be in sinusrhythm as long as there are coordinated atrial contractions, followed by normal ventricular contractions. This can be demonstrated on an electrocardiograph by a P-wave preceding each QRS-complex, with normal intervals.

The normal heart rate ranges from 60 – 100 beats per minute. Some individuals who are athletically inclined may have a resting heart rate less than 60 beats per minute. This sinusbradycardia can be a normal variant; however, there are pathological causes of these findings. A pathological example of this is sicksinussyndrome (also called sinoatrial disease), which is an age-related degeneration, or ischaemic injury, of the sinoatrial node resulting in fibrosis of the specialized myocardium. In addition to sinus bradycardia, patients may also experience dizziness, palpitations, and syncopal episodes as a result of periodic sinus arrest and atrial or ventricular arrhythmias.

Atrial Tachyarrhythmia

Atrial tachyarrhythmias are a group of disorders characterized by an abnormally high atrial contraction rate (>100 beats per minute). These contractions are often uncoordinated and ineffective, resulting in a reduction in ventricular filling. These forms of tachycardia are typically associated with ectopicfoci that are being propagated within an abnormal electrical circuit. The two most common types of atrial tachyarrhythmias include atrial fibrillation and atrial flutter.

Atrial Fibrillation

Atrialfibrillation is commonly a disorder of older individuals; with prevalence rates (of initially around 0.5%) that increase with age (roughly 9% of individuals > 80 years old). The pathophysiology behind atrial fibrillation is such that there is abnormalautomaticity, usually originating from the pulmonary veins or abnormal atrial tissue, which propagates around reentrant electrical loops within the atria. The presence of a re-entrant pathway, and the constant ectopic firing, contributes to the chronicity of the arrhythmia.

Atrialdilatation and ischaemictissue facilitate the development of re-entrant circuits. The dilatation results in stretching of the electrical pathway, which slows down the propagation of an action potential through a particular loop. As a result, some of the tissues exit the normal post action potential refractory period (i.e. completing repolarization) and can, therefore, be prematurely depolarized by an ectopic beat. The myocardium heals by forming fibrous tissue, which is a poor conductor of electricity. Consequently, the action potential has to find an alternative (possibly longer) route to travel; which leads to a similar situation described above.

The ineffective, uncoordinated, rapid activities of the atria are transmitted to the ventricles via the atrioventricular node. Inadvertently, because these impulses are poorly coordinated, the atrioventricularnode is irregularly activated. Therefore, patients with atrial fibrillation have a characteristic irregularly irregular (irregularintermittent) pulserate. Not only are these pulsations irregular, but they occur at varying intervals. The electrocardiograph of a patient with atrial fibrillation will reveal irregular ventricular activity and irregular atrial activity in the form of fibrillationwaves. Therefore, there is no clear relationship between atrial and ventricular activity. For completion, a patient may also have a regularly irregular (regular intermittent) pulse rate. Although these pulsations are irregular, they occur at typical intervals. Patterns like this can be observed in sinus arrhythmias or second degree heart blocks.

Atrial fibrillation occurs in one of three forms:

Paroxysmal atrial fibrillation lasting for up to seven days then spontaneously aborting,

Shortly after the onset of electrical abnormality, the heart is likely to undergo electrical remodeling. If it persists for months, then structural remodeling of the heart will occur. For this reason, atrial fibrillation is regarded as a progressive disorder, such that patients with paroxysmal disease are likely to progress to permanent atrial fibrillation over time.

Unfortunately, atrial fibrillation is associated with significant morbidity (syncopal episodes, palpitations, precipitation of underlying heart disease) and mortality (commonly caused by stroke). The poor atrial contraction leads to hemostasis within the atria. Hemostasis favors blood clot formation (recall Virchow’s triad) typically within the left atrial appendage; where these clots can cause a thromboembolicevent.

In light of these potentially catastrophic events, the mainstay of treatment for these patients includes rhythmcontrol (chemically with beta blockers and/or class III antiarrhythmic agents or electrically with direct current defibrillation), ratecontrol (with beta blockade, digoxin, or verapamil), and thromboembolismprophylaxis (with warfarin or a novel oral anticoagulant such as dabigatran). Catheter ablation of the abnormal electrical circuit is also a treatment option for patients with atrial fibrillation that is refractory to medical therapy.

Atrial Flutter

In contrast to atrial fibrillation, which is associated with ectopic foci, atrial flutter arises as a result of large reentry circuits within the region of the tricuspid annulus of the right atrium. Additionally, the atrial tachycardia of roughly 300 beats per minute is associated with a variable atrioventricular blockade. The atrial beats are conducted to the ventricles and may result in hemodynamic instability. The electrocardiograph displays a pathognomonic feature of ‘saw-toothed’ atrial activity; which may be confounded by the associated atrioventricular blocks. This particular abnormality should be a top differential for patients with electrocardiographs that show narrow complex tachycardia with a rate > 150 beats per minute.

Chemical (amiodarone) or electrical (direct current defibrillation) cardioversion may help with restoring normal rhythm, while rate control is achieved with either beta blockers , digoxin, or verapamil. Both amiodarone and beta blockers have been shown to prevent recurrence of atrial flutter. Catheter ablation is the definitive treatment option; offering a complete cure in up to 90% of the patients.

Atrial Enlargement

Atrial enlargement refers to increase in the volume of the atria. This is always a pathological process that can affect both atria. However, it is more common for left atrial enlargement to occur than it is for the right atrium to enlarge. Any condition that increases the pressure exerted on the atria can result in atrial enlargement. Therefore, the spectrum of etiological factors that causes atrial enlargement includes (but is not limited to) septal defects, valvulopathies, and hypertension (both systemic and pulmonary).

Left Atrial Enlargement

Left atrial enlargement is more commonly encountered than right atrial enlargement, mainly because the causes of left atrial enlargement are more common. The causes can be divided into congenital (such as ventricular septal defects or patent ductus arteriosus) or acquired causes (such as left ventricular hypertrophy or mitral incompetence secondary to chronic hypertension, or mitral stenosis).

Another way to group the causes of left atrial enlargement is to consider causes that result in volume overload in the atrium (septal defects, patent ductus arteriosus, and mitral regurgitation) and those that result in an increase in the left atrial pressure (chronic hypertension, mitral stenosis, and left ventricular hypertrophy). Independent from the cause, the end result is stretching of the atria. The progressive dilatation has been marked as an independent risk factor for increased mortality and morbidity as this phenomenon is associated with both atrial fibrillation and thromboembolic events (discussed earlier), as well as pulmonary hypertension.

In addition to the complications of atrial fibrillation and thromboembolism, patients may also experience left recurrent laryngeal nerve palsy (Ortner syndrome) and difficulty swallowing in severe cases (dysphagia megalatriensis) as a result of the mass effect of the enlarged left atrium. On the electrocardiogram, bifid P-waves (with at least 1 small box – 0.04 seconds between the two peaks) and a total increase in P-wave duration (about 0.11 seconds) are seen in lead II. Lead V1 will show a biphasic P-wave, with the negative portion (corresponding to left atrial depolarization) being at least 1 mm deeper. However, definitive diagnosis is best made with echocardiography, where the actual volume of the atrium can be measured.

Right Atrial Enlargement

Like left atrial enlargement, right atrial enlargement will result from increased blood volume or pressure within the atrium. An increase in right atrial pressure can result from pumping against stenotic tricuspid or pulmonary valves, hypertrophied right ventricle, or transmitted pressure increases from pulmonary hypertension (secondary to chronic lung disease). An atrial septal defect with a left to right shunt can also result in an increase in transmitted pressure to the right atrium.

An incompetent tricuspid valve (either due to primary valve disease or as sequelae of dilated cardiomyopathies) can result in an increase in the volume of blood passed into the right atrium. The consequences are similar to those observed in mitral valve incompetence in right atrial dilatation. While echocardiography will be the appropriate test for a definitive diagnosis, there are key features of the electrocardiography that will support the diagnosis. These changes include an increase in the amplitude of the P-wave in the inferior leads (> 2.5 mm) and in precordial leads V1 and V2 (>1.5 mm).

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